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Advances in Nutrition and Cancer

Overview of attention for book
Advances in Nutrition and Cancer
Springer Berlin Heidelberg

Table of Contents

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    Book Overview
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    Chapter 1 The Role of Metabolic Carcinogenesis in Cancer Causation and Prevention: Evidence from the European Prospective Investigation into Cancer and Nutrition.
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    Chapter 2 Obesity, Energy Balance, and Cancer: A Mechanistic Perspective.
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    Chapter 3 Fruits and Vegetables: Updating the Epidemiologic Evidence for the WCRF/AICR Lifestyle Recommendations for Cancer Prevention.
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    Chapter 4 The diet as a cause of human prostate cancer.
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    Chapter 5 Mediterranean Dietary Pattern and Chronic Diseases.
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    Chapter 6 Dietary Salt Intake and Risk of Gastric Cancer.
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    Chapter 7 Alcoholic Beverages and Carbonated Soft Drinks: Consumption and Gastrointestinal Cancer Risks.
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    Chapter 8 Anti-Inflammatory and Anticancer Drugs from Nature.
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    Chapter 9 Selenium and Cancer: A Story that Should not be Forgotten-Insights from Genomics
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    Chapter 10 Resveratrol: From Basic Studies to Bedside.
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    Chapter 11 Quercetin: A Pleiotropic Kinase Inhibitor Against Cancer.
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    Chapter 12 Sulforaphane as a Promising Molecule for Fighting Cancer
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    Chapter 13 Functions, Aberrations, and Advances for Chromatin Modulation in Cancer.
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    Chapter 14 Epigenetics and Epidemiology: Models of Study and Examples.
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    Chapter 15 Dietary Epigenetics in Cancer and Aging
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    Chapter 16 Breast Cancer and the Importance of Early Life Nutrition
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    Chapter 17 Olive Oil and Other Dietary Lipids in Breast Cancer.
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    Chapter 18 A Holistic Approach to Study the Effects of Natural Antioxidants on Inflammation and Liver Cancer.
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    Chapter 19 Extra Virgin Olive Oil: From Composition to "Molecular Gastronomy"
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    Chapter 20 Life Style Prevention of Cancer Recurrence: The Yin and the Yang.
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    Chapter 21 New Perspective for an Old Antidiabetic Drug: Metformin as Anticancer Agent.
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    Chapter 22 Gut Microbes, Diet, and Cancer.
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    Chapter 23 Advances in Nutrition and Cancer
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    Chapter 24 Nutriomes and Personalised Nutrition for DNA Damage Prevention, Telomere Integrity Maintenance and Cancer Growth Control
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    Chapter 25 Novel Approaches in Melanoma Prevention and Therapy.
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    Chapter 26 Concluding Remarks.
Attention for Chapter 4: The diet as a cause of human prostate cancer.
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Citations

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Chapter title
The diet as a cause of human prostate cancer.
Chapter number 4
Book title
Advances in Nutrition and Cancer
Published in
Cancer treatment and research, October 2013
DOI 10.1007/978-3-642-38007-5_4
Pubmed ID
Book ISBNs
978-3-64-238006-8, 978-3-64-238007-5
Authors

William G Nelson, Angelo M Demarzo, Srinivasan Yegnasubramanian, Nelson WG, Demarzo AM, Yegnasubramanian S, William G. Nelson, Angelo M. DeMarzo, Nelson, William G., DeMarzo, Angelo M., Yegnasubramanian, Srinivasan

Editors

Vincenzo Zappia, Salvatore Panico, Gian Luigi Russo, Alfredo Budillon, Fulvio Della Ragione

Abstract

Asymptomatic prostate inflammation and prostate cancer have reached epidemic proportions among men in the developed world. Animal model studies implicate dietary carcinogens, such as the heterocyclic amines from over-cooked meats and sex steroid hormones, particularly estrogens, as candidate etiologies for prostate cancer. Each acts by causing epithelial cell damage, triggering an inflammatory response that can evolve into a chronic or recurrent condition. This milieu appears to spawn proliferative inflammatory atrophy (PIA) lesions, a type of focal atrophy that represents the earliest of prostate cancer precursor lesions. Rare PIA lesions contain cells which exhibit high c-Myc expression, shortened telomere segments, and epigenetic silencing of genes such as GSTP1, encoding the π-class glutathione S-transferase, all characteristic of prostatic intraepithelial neoplasia (PIN) and prostate cancer. Subsequent genetic changes, such as the gene translocations/deletions that generate fusion transcripts between androgen-regulated genes (such as TMPRSS2) and genes encoding ETS family transcription factors (such as ERG1), arise in PIN lesions and may promote invasiveness characteristic of prostatic adenocarcinoma cells. Lethal prostate cancers contain markedly corrupted genomes and epigenomes. Epigenetic silencing, which seems to arise in response to the inflamed microenvironment generated by dietary carcinogens and/or estrogens as part of an epigenetic "catastrophe" affecting hundreds of genes, persists to drive clonal evolution through metastatic dissemination. The cause of the initial epigenetic "catastrophe" has not been determined but likely involves defective chromatin structure maintenance by over-exuberant DNA methylation or histone modification. With dietary carcinogens and estrogens driving pro-carcinogenic inflammation in the developed world, it is tempting to speculate that dietary components associated with decreased prostate cancer risk, such as intake of fruits and vegetables, especially tomatoes and crucifers, might act to attenuate the ravages of the chronic or recurrent inflammatory processes. Specifically, nutritional agents might prevent PIA lesions or reduce the propensity of PIA lesions to suffer "catastrophic" epigenome corruption.

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X Demographics

X Demographics

The data shown below were collected from the profile of 1 X user who shared this research output. Click here to find out more about how the information was compiled.
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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 55 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Colombia 1 2%
Unknown 54 98%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 9 16%
Student > Bachelor 8 15%
Student > Master 7 13%
Researcher 4 7%
Professor 3 5%
Other 7 13%
Unknown 17 31%
Readers by discipline Count As %
Medicine and Dentistry 16 29%
Agricultural and Biological Sciences 6 11%
Biochemistry, Genetics and Molecular Biology 4 7%
Nursing and Health Professions 3 5%
Engineering 2 4%
Other 6 11%
Unknown 18 33%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 2. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 30 July 2022.
All research outputs
#17,621,300
of 26,626,316 outputs
Outputs from Cancer treatment and research
#99
of 195 outputs
Outputs of similar age
#138,931
of 225,924 outputs
Outputs of similar age from Cancer treatment and research
#13
of 17 outputs
Altmetric has tracked 26,626,316 research outputs across all sources so far. This one is in the 31st percentile – i.e., 31% of other outputs scored the same or lower than it.
So far Altmetric has tracked 195 research outputs from this source. They typically receive more attention than average, with a mean Attention Score of 9.1. This one is in the 47th percentile – i.e., 47% of its peers scored the same or lower than it.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 225,924 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 36th percentile – i.e., 36% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 17 others from the same source and published within six weeks on either side of this one. This one is in the 23rd percentile – i.e., 23% of its contemporaries scored the same or lower than it.